These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Role of calcium-calmodulin-dependent protein kinase II in modulation of sensorimotor synapses in Aplysia.
    Author: Nakanishi K, Zhang F, Baxter DA, Eskin A, Byrne JH.
    Journal: J Neurophysiol; 1997 Jul; 78(1):409-16. PubMed ID: 9242289.
    Abstract:
    The Ca2+-calmodulin-dependent protein kinase II (CaMKII) inhibitor, [1-[N,O-bis(5-isoquinolinesulfonyl)-N-methyl-L-tyrosyl]-4-phenylpiperazi ne) (KN-62), was used to investigate the role of CaMKII in synaptic transmission and serotonin (5-HT)-induced facilitation in Aplysia. Application of KN-62 (10 microM) by itself increased the amplitude of excitatory postsynaptic potentials (EPSPs) at sensorimotor synapses in pleural-pedal ganglia. Moreover, in the presence of KN-62, 5-HT-induced short-term facilitation was attenuated. Application of KN-62 by itself slightly increased the duration of action potentials in isolated sensory neuron somata but did not block spike broadening produced by 5-HT. KN-62 had no effect on excitability of isolated sensory neuron somata nor did it block 5-HT-induced enhancement of excitability. These results indicate that the attenuation of short-term facilitation by KN-62 is not due to modulation of the membrane currents contributing to 5-HT-induced spike broadening or enhancement of excitability. Rather, these data are consistent with the hypothesis that CaMKII contributes to the regulation of sensorimotor connections and that it has a role in spike-duration-independent processes contributing to short-term facilitation.
    [Abstract] [Full Text] [Related] [New Search]